149 Endocarditis

Question 1

Endocarditis

Answer 1

Noninfective endocarditis

• •Nonbacterial thrombotic endocarditis (NBTE, marantic endocarditis)
• •Rheumatic endocarditis
• •Libman-Sacks endocarditis (manifestation of systemic lupus erythematosis (SLE)

Infective endocarditis

Question 2

Nonbacterial Thrombotic Endocarditis

Answer 2

• Definition: The deposition of small masses of fibrin, platelets, and other blood components on leaflets of cardiac valves.
  
  • Lesions do not contain microorganisms
  • Valvular damage not a prerequisite; valves usually previously normal
• Pathogenesis
  
  • Subtle endothelial abnormalities
  • Hypercoagulable states
  • malignancies (especially adenocarcinomas) found in 50% of cases
• Morphologic Features
  
  • small nodules on lines of valve closure
  • nodules may be bulky and friable
  • valve leaflets otherwise normal
  • aortic valve most common, mitral valve next most frequently involved

Question 3

Infective Endocarditis

Answer 3

• Definition: Infection of the cardiac valves or mural surface of the endocardium, with formation of adherent mass of thrombotic debris and organisms, termed a “vegetation”.
  
  • Any microorganism may be present, but most cases are bacterial
• Acute Endocarditis
  
  • –High virulence organisms: may affect normal valves
    
    • •Staphylococcus aureus
  • rapid destruction, no inflammatory response, embolize infarct
• •Subacute Endocarditis
  
  • –Lower virulence organisms: affects previously abnormal valves
    
    • •alpha-hemolytic streptococci
  • Less firm than acute, cause less valve damage, systemic emboli
• •Pathogenesis
  
  • –Organisms implanted during bacteremia
  • –Conditions which increase risk: preexisting cardiac abnormalities, Endothelial injury, Turbulent flow (due to scarred valve of congenital heart defect, e.g. V.S.D.), prosthetic heart valves, intravenous drug abuse

Question 4

Fungal endocarditis

Answer 4

• Prosthetic valves are especially susceptible to colonization since it is a foreign material
• Common location around sewing ring
• Also frequently involved with sterile thrombotic vegetations

Question 5

Acute Rheumatic Carditis

Answer 5

•Endocardium

–Most pronounced in mitral & aortic valves

–Inflammation, edema, fibrinoid necrosis

–Aschoff nodules not common

–Verrucous endocarditis

• Small excrescences along lines of valve closure
• Lesions may resolve or undergo fibrosis

Anitschkow cells are found in Aschoff nodules

They are histiocytes with vesicular nuclei and abundant cytoplasm

Nuclei resemble owl eyes!

Question 6

Causes of mitral stenosis

Answer 6

Postinflammatory scarring (rheumatic heart disease)

Question 7

Causes of mitral valve regurgitation

Answer 7

Question 8

Mitral Valve Prolapse

Answer 8

–Most common cause of isolated mitral regurgitation

–Affects women > men

–Mitral valve “floppy” or incompetent

–May occur with Marfan’s syndrome

–Mitral valve cusps (especially posterior cusp) soft, enlarged, and ballooned into left atrium during systole

–Cordae may rupture

–Loose, edematous, basophilic ground substance in valve leaflets and chordae

•Identified by midsystolic click

Question 9

Aortic Stenosis + causes

Answer 9

•Most frequent valvular abnormality

•Acquired >> congenital

•Senile calcification, degenerative, “wear and tear” > 10% due to rheumatic fever

1-2% congenitally bicuspid

•Heaped-up calcified masses in sinuses of Valsalva

1. •Postinflammatory scarring (rheumatic heart disease 30-60 yrs old)
2. •Senile calcific aortic stenosis (>60yrs)
   
   • Heaped up calcifications in the sinus of Valsalva
   • Moderately thickened free edge
   • Absence of fusion of the commisures
3. •Calcification of congenitally deformed valve (30-50yrs)

• Thickening of the free edges of the valve cusps
• Fusion of the cusps
• Normal sinus of Valsalva

Question 10

Causes of aortic regurgitation

Answer 10

Question 11

Ankylosing spondylitis

Answer 11

• •Systemic disease affecting joints, lungs, heart and eyes.
• •Inflammation can involve the aorta and heart
• •Can cause aortic regurgitation due to dilatation of the aorta and scarring of valve cusps

Question 12

Pericardial Physiology

Answer 12

• •not needed to sustain life
• •physiologic functions
  
  • –limit cardiac dilatation
  • –maintain normal ventricular compliance
  • –reduce friction to cardiac movement
  • –barrier to inflammation
  • –limit cardiac displacement

Question 13

Pericardial Inflammation
pathogenesis

Answer 13

1. •Contiguous spread
   
   • –lungs, pleura, mediastinal lymph nodes, myocardium, aorta, esophagus, liver
2. •Hematogenous spread
   
   • –septicemia, toxins, neoplasm, metabolic
3. •Lymphangetic spread
4. •Traumatic or irradiation

• •Inflammation provokes a fibrinous exudate with or without serous effusion
• •The normal transparent and glistening pericardium is turned into a dull, opaque, and “sandy” sac
• •Can cause pericardial scarring with adhesions and fibrosis

Question 14

Causes of Pericarditis

Answer 14

• Rheumatic Fever
• Scleroderma
• Postcardiotomy
• Drug-hypersensistivity reaction
• Systemic lupus erythematosus
• Postmyocardial infarction (Dressler) syndrome

Question 15

Dressler’s Syndrome

Answer 15

•Described by Dressler in 1956

•fever, pericarditis, pleuritis
(typically with a low grade fever and a pericardial friction rub)

• occurs in the first few days to several weeks following MI or heart surgery
• incidence of 6-25%
• treat with high-dose aspirin

Question 16

Constrictive Pericarditis

Answer 16

• An uncommon post inflammatory disorder
• the encasement of the heart by a rigid, nonpliable pericardium
• characterized by a thickened, fibrotic, and frequently calcified pericardium
• rarely develop after an episode of acute idiopathic pericarditis
• more likely to develop after subacute pericarditis with effusion that evolve over several weeks

Question 17

Etiologies of Cardiac Tamponade

Answer 17

• Fluid accumulation within the pericardial space resulting in increased intracardiac pressure
• Progressive limitation of ventricular diastolic filling
• Reduction of stroke volume and cardiac output

Question 18

Effect of volume and timing of fluid accumulation on intrapericardial pressure/tampanode

Answer 18

Question 19

Beck’s Triad

Answer 19

•Described in 1935 by thoracic surgeon Claude S. Beck

3 features of acute tamponade

1. –Decline in systemic arterial pressure
2. –Elevation in systemic venous pressure (e.g. distended neck vein)
3. –A small, quiet heart